Fatal ungulate disease advances as Wyoming game managers continue on in denial-

Our recent story on chronic wasting disease (CWD) in Wisconsin now has a followup in the treasured Greater Yellowstone country. In both places, wildlife managers and politicians continue to take a heedless attitude toward the always fatal elk, deer and moose disease,  and fail to take action. States like Wyoming have massive winter elk feeding programs that dangerously concentrate the elk, inviting CWD to take hold. Other states like Idaho, have numerous elk farms and elk shooting ranches similar to those that have spread the disease into many states and provinces of Canada.

The Greater Yellowstone Coalition just issued a map and news release about CWD’s relentless spread to the northwest across Wyoming.

– – – – – –

News Release

May 14, 2013

Fatal disease of Wyoming deer and elk moves west and north

For more information contact:
Lloyd Dorsey, Greater Yellowstone Coalition, 307 734 6004; Bruce Smith, PhD, USFWS (retired): 406 842 5995

JACKSON, Wyo. Information gleaned from the Wyoming Game & Fish Department indicates that deadly Chronic Wasting Disease (CWD) is advancing towards western Wyoming’s winter elk feedgrounds and Yellowstone National Park.

A new map from the Greater Yellowstone Coalition shows the areas where the disease has been detected in the Greater Yellowstone Ecosystem are within 45 miles of winter elk feedgrounds and about 40 miles from Yellowstone Park’s northeast corner. The 2012 information reveals the farthest advance west of CWD in deer in Wyoming yet. Last year, three mule deer were found infected with CWD in Green River, Wyo.; an infected moose was found near Idaho in Star Valley, Wyo., in 2008.

Veteran conservationist Lloyd Dorsey of the Greater Yellowstone Coalition said the disease is now essentially on the doorstep of the elk feedgrounds, including the National Elk Refuge in Jackson Hole. Dorsey notes that deer from the endemic disease areas to the east and south migrate north and west to elk herd units in the upper Green River and Jackson Hole, where most of the winter feedgrounds are located.

Wildlife managers continue to play Russian roulette with our treasured game herds by baiting and feeding them unnecessarily, Dorsey said. “The steady advance of the disease should serve as a strong message to eliminate dense concentrations of elk by phasing out artificial winter feeding. We must break the cycle of disease ó before it harms some of America’s great elk herds.”

The disease also is moving inexorably closer to Yellowstone Park through the Big Horn Basin, where it is approximately 40 miles away from the park boundary. So far no elk have been detected with the disease in Yellowstone and Grand Teton national parks or the National Elk Refuge. According to agency accounts, hunter harvested elk and some that appear to be sick are tested for the disease.

The good news is that the disease has not been detected at the feedgrounds or national parks yet, said Bruce Smith, retired U.S. Fish & Wildlife Service biologist and former senior biologist at the National Elk Refuge. Managers can still act to responsibly phase out winter feeding of elk and limit the effects of this and other diseases.

CWD is a degenerative disease of the central nervous system and brain, and can infect elk, deer and moose. It is always fatal and there is no cure. The same disease can infect all these species and is transmissible from one species to another. Experts say that artificially concentrating herds by winter feeding increases the risk of such diseases, and recommend that deer and elk not be artificially fed or baited during winter in order to keep them spread out as much as possible.

For more information on the map depicting CWD areas and Greater Yellowstone Coalition’s efforts to phase out the artificial elk feeding areas and transition to healthier, free ranging wildlife, see http://www.greateryellowstone.org/elkrefuge


About The Author

Ralph Maughan

Dr. Ralph Maughan is professor emeritus of political science at Idaho State University. He was a Western Watersheds Project Board Member off and on for many years, and was also its President for several years. For a long time he produced Ralph Maughan's Wolf Report. He was a founder of the Greater Yellowstone Coalition. He and Jackie Johnson Maughan wrote three editions of "Hiking Idaho." He also wrote "Beyond the Tetons" and "Backpacking Wyoming's Teton and Washakie Wilderness." He created and is the administrator of The Wildlife News.

40 Responses to Chronic Wasting Disease closes in on Yellowstone

  1. I knew the guy that did the environmental impact study about shutting down the National Elk Refuge a decade ago. He was of the mind after dealing with the powers that be, that as important as it is to do, it is such a political football that no one has the will to go forward. The general public won’t get on board until after 3/4th of the elk on the refuge are dead from chronic wasting. Only then will they understand and be willing to the solution.

    • Ralph Maughan says:


      You are, unfortunately, probably right, though I hope not. Then it will too late because CWD prions are almost indestructible, lying in the soil indefinitely.

    • Robert R says:

      Daryl your exactly right!!
      Sportsman will get the blame for most if not all.

    • WyoWolfFan says:

      If CWD reaches the National Elk Refuge I wonder what that will do with tourism in the area.

  2. Ron says:

    I find it interesting that you seem to blame the deer and elk farms for the spread of CWD. Are you aware that there are NO elk or deer farms in Wyo. and there never has been. Wyo. has never licensed any deer or elk farms but CWD has been there for a long long time. Food for thought.

    • Ken Cole says:

      There may not be any deer or elk farms in Wyoming but there were in Colorado where this particular outbreak originated. See: http://www.cwd-info.org/pdf/34419a38.pdf

      And this: http://www.cwd-info.org/index.php/fuseaction/about.timeline

      • cobackcountry says:

        CWD can’t be kept in a pen. Once a diseased animal has encountered it, they don’t know boundaries. They roam. The prions are crazy strong. Deer, who are famous for blasting snot on everything around them, wander far and wide. Every where there is ungulate feces there will be CWD. It is a matter of time. They need to close the feed lots….or they’ll need to figure out how to rebuild herds from a real loss, due to this real threat.

        • cobackcountry says:

          They’d also need to figure out how to keep animals out of any area that there was ever CWD, because it (like Ralph said) never leaves the soil.

        • Ron says:

          You are correct there are Elk farms in Colorado but CWD was found in a Colorado Division Of Wildlife reasearch facility at the CSU campus in Fort Collins. Now the higest consentration of CWD is in Boulder Co. and Estes Park Co where there are no Elk farms and never has been. So who gave or spread CWD to who ????

  3. Ken Cole says:

    When a real threat to elk and deer arises, like this one, it seems that there is utter silence from those who are hysterical about wolves and the relatively minor impact they have caused. If you really are worried about the loss of deer and elk then I recommend getting hysterical about this issue over wolves. The impacts of this will likely be much more devastating.

  4. cobackcountry says:

    They absolutely will be worse Ken. I agree. There is evidence to support that earlier culling could keep prion transfer from occurring. There may be a window when the animals infected are not infectious. There may also be evidence that animals (mountain lions are the primarily studied predator that I have read up on)can detect symptoms humans don’t yet see or cannot yet detect.
    It would seem more prudent to worry about CWD then the scarcely populated wolves.

  5. Kirk Robinson says:

    And when the ungulate herds begin their inexorable decline, not only will it be too late to save them, but guess what type of species will get blamed for it – or at least become victims of “the one thing we sportsmen conservationists can do to save the herds from total decimation”?

  6. Immer Treue says:

    The time of the game farm, majestic herd mentality is over. In evolutionary terms, the numbers and proximity to each other of these animals never occurred until mid last century.

    Folks up here say wolves get mange Because there are too many of them. There a die off, and then the wolves are okay…

    I don’t know how many times Ive heard there are more deer in this country now than when Columbus got here. Nature in it’s own way, takes care of itself. Too much of a good thing is no longer good.

  7. greetings,

    some of you may not have seen this, and i thought you might find interest. …

    Wednesday, May 15, 2013

    Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay

    Research Article


    kind regards,

    • Ralph Maughan says:

      Terry Singeltary,

      So reading parts of your link above to numerous studies, I gather, as I had believed already, that CWD can reside in clay indefinitely and can be inhaled and infect deer as they forage with their nose to the ground.

      • cobackcountry says:


        That is absolutely correct. So it is existing at many levels of contact, from the ground up.

  8. CodyCoyote says:

    PRIONS are deformed proteins. They are in utter stark contrast to all other forms of pathogenic disease transmission, such as viruses, bacteria, toxicants, etc. Insidiously , they seem to prefer disupting neural tissue…brains and nerves. Prions are extremely stable and can persist for a very very long time. Yes, they do like clay monerals and can stay viable in them for a very long time. Animals excrete prions in manure and urine. Any means of ingesting prions is sufficient to unleash their destructive workings. They are pure genetic evil. Think undead Zombies.

    Yet they were unknown or at least unstudied before 1960. DNA discoverer and geneticist Francis Crick studied them in the late 60’s and published a seminal paper on them. Prions are really scary all around.

    One thing I am pretty sure about prions : Wyoming Game & Fish is in denial about them. CWD is marching onwards thru the herds…recall the Moose that were diagnosed with CWD a few years ago not that far from the National Elk Refuge.

    About all we can hope for to contain the spread are canny packs of wolves, and hungry grizzlies and cougars preying on the weak and crippled animals infected with CWD. Yet when I asked the Bill Rudd, Wyo G&F top guy explaining Wyoming’s first wolf plan to the crowd in Cody back in 2008 , if he saw any positive value to wolves, such as mitigating the spread of CWD, he categorically stated that the Department saw no positive value to having wolves since they were ” foisted onto Wyoming by the Feds”. ( paraphrasing his quote).

    Oh well. What else is new?

    • WM says:


      I am not so sure WY G&F is in denial. Something you have not seen, perhaps?


      I expect every state wildlife agency has it on their radar screen. The questions are what to do about it and when, since so little is known.

      And, RMEF and other private entities are VERY concerned as well. Someone (Ken?) pointed to an article written by Hal Herring in RMEF’s magazine, BUGLE, about 2003. Herring has written quite a bit over the years, state game regulations in many states seem to mention it quite a bit.

      I even expect WDFW in WA has considered implications to their elk feeding operations, as I suspect it has been addressed in ID and the National Elk Refuge as well. The question is balancing the risk, and some of us just don’t feel comfortable with where the balance point is at this time. The stakes are huge for so many reasons.

      • Kirk Robinson says:

        The idea that we can always find a technological fix for the problems that previous technology/ways of doing things cause – in this case a vaccine for inoculating ungulates against CWD, the spread of which is most likely caused by artificial crowding of animals – seems on the face of it to be a dubious one at best. Who knows what costs and additional problems a vaccine against CWD, implemented widely, will in turn cause? I guess prions don’t mutate like genes, but I think we can be quite sure that such a program won’t turn out to be a “silver bullet”. why not go with the tried and true instead: healthy populations of large carnivores and closing the feedlots and elk farms? That’s what common sense and science both suggest.

        I once asked Paul Paquette if he thought healthy populations of wolves would be effective in preventing the spread of CWD and he unhesitatingly said “Yes.”

        Why all of this fuss and trouble just to try to maximize the number of deer, elk and moose for “hunters” to take and to provide a stable predictable number year to year? Such hubris – and in my opinion, stupidity. It’s time to replace the North American Wildlife Conservation Model with something more scientifically and ethically sound – something that shows greater respect for the workings of untrammeled nature (or relatively untrammeled if you prefer). Hunting can still be part of the model.

        It is a great irony that the very methods that wildlife managers use to try to maximize and stabilize yield end up working to the opposite effect. That appears to be what is happening here. And, to cite another example of this irony, many of you are no doubt aware of the research showing that four or five decades of RM bighorn sheep trophy hunting in B.C. has reduced the size of the animals and the weight of the horns by something like 30%.

      • CodyCoyote says:

        WM- Maybe ” denial” was the wrong term to use. But the question is a valid one : beyond testing hunter-killed Deer for CWD at the few check stations still used during the fall hunting season , and issuing some infomercial stories , what exactly has Wy G&F actually DONE about CWD in areas where it is known or suspected of happening?

        We had a CWD outbreak in the Owl Creek Mtns south of me, another few cases reported over on the east side of the Big Horn Basin in the Lovell and Tensleep area, and they did little. I go by actions, not words.

        This I do know…Wyo G&F answers to rancherilandowners above and before all else. Which is why getting rid of the feedgrounds in western Wyoming has been a political impossibility. Ranchers want those elk bunched up and fed so they don’t mooch off pastures and grazeable lands in the winter . Ranchers honestly believe wildlife are eating THEIR grass, and livestock trumps wildlife. That is a two edged sword, if the feedgrounds become incubators and distributors of zootic pathogens.

        Today there is a story about Bison msyteriously dying in the rpesence of domestic sheep just north of Yellowstone NP. It is suspected but not yet shown that the sheep gave the bison a deadly fever that they themselves are immune to. The domestic sheep are new to that immediate area, and now bison are keeling over.

        We will get nowhere resolving any of these issues unless and until we put wildlife on an equal footing with domestic livestock in areas where they overlap.

        It ain;t happening in Wyoming, and it’s worse in Montana.

      • Ralph Maughan says:

        There is a big drum (barrel) on the Elk Refuge where hunters are urged to deposit elk heads for veterinary inspection.

        I have a photo of it somewhere.

  9. alf says:

    On the brighter side, scavengers will have it pretty easy

  10. cobackcountry says:


    I have visited the holding pens. CWD afflicted animals are currently penned there and are studied with great scrutiny. Additionally, these animals re intentionally fed to a study group of mountain lions. The lions show NED.

    If you look at this link, it gives specifications for handling any animals which you contact that may be infected. Maybe we can get I, maybe not. But when there are recommendations that say to wear rubber gloves and to bleach anything coming in contact with the animal….I’d say safe I better than sorry.

    Due in large par to CSU’s studies, there are faster ways to test animals for CWD. Initially, tests were only able to be done on necropsy of brain tissue. Now they can detect it earlier on tonsils of deer. They are making strides. There is no easy answer though ad we could very well lose huge numbers of animals before we have the solutions.

    At this point though, closing feed lots and letting predators cull sick animals sooner so as not to spread CWD even more…seems like common sense.

    • Greetings cobackcountry et al,

      i have corresponded with Dr. Miller about the mountain lion cwd study, and to date (11-17-2012), they show no signs of CWD. however, again, in my opinion, i think that any use of any species to cull out cwd in cervids would be very foolish. these predators would for certain spread the TSE agent, and then, you have to worry about the predators themselves and susceptibility to the CWD strains. felines and canines are susceptible to the CWD TSE prion, as are most species, even the rabbit fell to the TSE prion recently, anothor species thought to be resistant, but turns out NOT so.


      i kindly remind everyone of what one of the top BSE prion Gods said long ago, and believe it ;

      5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

      see full text ;


      see more here;


      so, never say never. …


      Friday, November 09, 2012

      *** Chronic Wasting Disease CWD in cervidae and transmission to other species


      some additional information on the CWD testing aspect of your post ;


      Ryan J. Monello1,6, Jenny G. Powers1, N. Thompson Hobbs2, Terry R. Spraker3, Katherine I. O’Rourke4,5 and Margaret A. Wild1

      + Author Affiliations

      1National Park Service, Biological Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins, Colorado 80525, USA

      2Natural Resource Ecology Laboratory and Graduate Degree Program in Ecology, Colorado State University, Fort Collins, Colorado 80523, USA

      3Colorado State Diagnostic Laboratory, College of Veterinary Medicine, Colorado State University, Fort Collins, Colorado 80523, USA

      4United States Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, 3003 Animal Disease Biotechnology Facility, Washington State University, Pullman, Washington 99164, USA

      ↵6 Corresponding author (email: Ryan_Monello@nps.gov)


      A reliable antemortem test is needed to understand the ecology of chronic wasting disease (CWD) in elk (Cervus elaphus nelsoni). We measured the ability of antemortem biopsy samples from the rectal mucosa to detect the abnormal prion protein associated with CWD (PrPCWD), the relationship between test results from the obex and rectal biopsies at varying stages of CWD progression, and the prevalence of CWD in free-ranging elk from Rocky Mountain National Park, Colorado, USA. We sampled and placed radio collars on 136 adult female elk in the winter of 2007–08. Elk with biopsy samples found positive for PrPCWD by immunohistochemistry (IHC) were euthanized and the obex and retropharyngeal lymph nodes were examined with IHC. We resampled, euthanized, and necropsied 20, 25, and 34 of the remaining study elk in each of the three following winters, respectively. Sensitivity of rectal biopsy samples increased in an asymptotic fashion with follicle count and was maximized at 85% (95% credible limits [CL]=60, 98) in the beginning of the study, when a greater proportion of elk were in a detectable stage of prion infection. However, maximum sensitivity was reduced to 72% (CL=46, 94) when we included resampled elk, which included recently infected elk that were initially negative using rectal biopsies and IHC. Test results were similar between rectal biopsies and the obex, but the earliest stages of prion infection were only detected by using retropharyngeal lymph nodes. Minimum CWD prevalence was estimated to be 9.9% (CL=5.7, 15.7) using rectal biopsies, but this rose to 12.9% (CL=8.0, 19.1) when we included four elk that were likely misdiagnosed at initial capture. Our results indicate rectal biopsies can provide a useful research tool for CWD in elk populations, but should be used with caution because they can miss individuals in early stages of infection and underestimate prevalence. Prevalence estimates from this population are the highest reported to date in elk and indicate that under appropriate conditions, CWD may be able to affect the dynamics of high-density elk populations.

      Biopsy Cervus elaphus chronic wasting disease Colorado CWD elk prion rectal mucosa

      Received December 22, 2011. Accepted October 9, 2012.

      © Wildlife Disease Association 2013


      Friday, August 24, 2012

      Diagnostic accuracy of rectal mucosa biopsy testing for chronic wasting disease within white-tailed deer (Odocoileus virginianus) herds in North America


      kind regards,

  11. i urge everyone interested and concerned about cwd, to read what the UK is doing to try and prevent the cwd strains from entering the UK from North America. Canada has already infected Korea with CWD via trade. the UK is very concerned. please see full report and followed up with additional link to additional science ;

    Friday, December 14, 2012

    DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

    Currently, there have been no reported cases of CWD or other TSE in deer in Great Britain (GB) or Europe. Given the consequences of CWD observed in North America, it is imperative that GB remains free of the disease. This risk assessment aims to assess the risk of CWD being imported into GB from North America and consequently, consider the risk of exposure and infection within the GB deer population. The assessment focuses on two main routes of entry including importation of animal feed and movement of contaminated clothing, footwear and equipment of tourists, deer hunters and British servicemen between affected areas of North America and GB. It is important to highlight that there are significant data gaps in this assessment. The main conclusions from this assessment are:


    In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

    Animals considered at high risk for CWD include:

    1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

    2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

    Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

    The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

    Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

    There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.


    36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

    The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

    Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.


    The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).


    In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.


    In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.


    Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.



    Friday, December 14, 2012

    DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012


    kind regards,

  12. cobackcountry says:

    I wonder, would CWD have impacted YNP herds by now were it not for wolves and other predators culling sick animals? I guess we may never know.

    • Kirk Robinson says:

      Good question, cobackcountry.

      In response to Mr. Singletary’s concern about using “any species to cull out CWD in cervids,” being very foolish: this can be taken two different ways. One, it could be understood to mean that we should try to protect large carnivores from preying on ungulates (how exactly, I don’t know – unless by removing them through hunting, which would seem a rather extreme solution; or two, it could mean that we would do well to try to prevent or reduce the spread of CWD in cervids, which makes a lot more sense and is therefore what I take him to be suggesting. But how should we go about doing that? By vaccinating cervids against CWD? Hypothetically, we might try that; but not as a substitute for getting rid of elk farms and feeding grounds. At least not in my opinion.

      • Kirk Robinson says:

        In response to Mr. Singletary’s concern about using “any species to cull out CWD in cervids,” being very foolish: this can be taken two different ways. One, it could be understood to mean that we should try to protect large carnivores from preying on ungulates (how exactly, I don’t know – unless by removing them through hunting, which would seem a rather extreme solution; or two, it could mean that we would do well to try to prevent or reduce the spread of CWD in cervids, which makes a lot more sense and is therefore what I take him to be suggesting. But how should we go about doing that? By vaccinating cervids against CWD? Hypothetically, we might try that; but not as a substitute for getting rid of elk farms and feeding grounds. At least not in my opinion.


        easy, you just do NOT _promote_ the use of predators as a CWD eradicator, as some have suggested. in nature, you can’t stop predators from chasing their kill, that’s nature. but by promoting predators as a CWD eradicator, would only enhance the spread of CWD further, in my opinion. …

        there is a vaccine in the works, not validated yet, we can only hope they perfect this very soon. please see ;

        Thursday, February 21, 2013

        Game and Fish Begins Study to Evaluate Chronic Wasting Disease Vaccine


        kind regards,

        • cobackcountry says:

          The trouble with vaccines are vast, like cost how to know which animals are vaccinated, methods of delivery.

          I get to work on a study dealing with these specific things. I hope to gain better insight and perhaps be a part of solutions.

          No matter what we can come up with, we can’t stop being precautious, and taking steps to limit the spread.

        • Kirk Robinson says:

          Sorry Mr. Singletary, but I can’t see how promoting predators as a means of combating CWD in cervids would instead promote the spread of CWD in cervids; unless, as I suggested for you, it were to impede the use of technological fixes, such as the use of vaccines.

          My fear, actually, is just the reverse of yours – that reliance on technological fixes might impede or undermine efforts to allow wild nature to do its magic. And I dare say that there is a huge disparity in the evidence regarding which is most likely to be successful: letting wild nature do its magic (predators and no feed lots) vs. untested vaccines. At this stage,the evidence is almost totally on the side of the first option. Why so much confidence in the vaccines anyway? Where is the evidence that that would be a superior remedy? Perhaps better yet, why not both – assuming folks would support both?

          • Ida Lupine says:

            My feelings also. Not that I’m adverse to a vaccine, but humans think they always know better than nature, and well-meaningly bungle things many times.

          • Kirk Robinson says:

            May 20, 2013 at 8:53 am

            Sorry Mr. Singletary, but I can’t see how promoting predators as a means of combating CWD in cervids would instead promote the spread of CWD in cervids; unless, as I suggested for you, it were to impede the use of technological fixes, such as the use of vaccines…snip…end


            Mr. Robinson,

            you brought vaccine possibilities up, i just posted the recent science on it for you. i never said i was for or against vaccines. personally, i think any vaccine for any TSE will not be seen validated in my lifetime.

            and second, the Louping-ill vaccine WAS the cause of some 18,000 scrapie infected sheep, due to the vaccine being made from scrapie infected sheep brains ;


            what about the children ???


            also, to promote predators to eradicate cwd, again, you have the potential for the predators to spread the cwd agent where ever they drag there kill off too, let alone expose that specific species and other species that may feed on that kill, to the CWD agent. again, just a foolish option in my opinion.

            if your _hoping_ for a slow eradication via predators as a possible solution, would it not be more swift for culling, and then proper disposal, to keep from further spreading ?

            you claim to let nature take it’s course on CWD, well, how is that working out in Wisconsin to date ? even with all their eradication efforts, cwd still is spreading, so to let nature take it’s course, when you have these shooting pens helping to trade and spread CWD all over, would be another foolish route to take, in my opinion.

            imagine what would have happend if that’s what they would have done in England with BSE, just said, let nature take it’s course. when man mucks things up so bad, you just can’t let nature take it’s course sometimes. you have to fix it, or nature can do you in.

            TSE prions know no boundries, they know no borders, and the prion knows no age limits, and it’s man that keeps this stupid disease going, in my opinion.

            another example of species and the TSE agent, look at the history of the zoo animals in the UK during the BSE crisis ;

            Below, the entire scientific literature of 46 papers on zoo TSE, many obscure and expensive to obtain, are summarized from full text. The overall picture that emerges is appalling — the British zoo cover-up has not only affected animals in their own zoos but also other zoos worldwide through the sale of contaminated speciality chows and through export and exchange of rare and endangered species involved in conservation programs.
            All the zoos involved are named by name here (unlike in the journal articles). Why protect a zoo that feeds cheetahs split spinal cords from cattle throughout the BSE epidemic? (Better to have tossed them the zoo veterinarian.) Names are important for zoos which would not want to export their healthy animals to these facilities or import possibly preclinical animals for their own endangered species breeding programs or release into wild populations. Medical scientists doing unrelated research want to know if animals in their programs are already incubating prion disease.

            Ravensden, Marwell, Chester, Port Lympne, London, Whipsnade, Woburn, and Edinburgh are 8 known BSE affected British zoos. Woburn Safari Park apparently killed the lion by feeding it split cattle spinal cords and skulls.





            Two cases of FSE have been diagnosed in imported animals in Australian zoos in 1992 (cheetah) and 2002 (Asiatic golden cat). In both cases exposure before importation to feeds derived from BSE affected cattle are thought to have caused the disease. In both instances, effective response measures were taken.


            Our unexpected finding that the same patterns of PrP distribution and brain degeneration were present in asymptomatic lemurs from two other French primate facilities suggests that BSE-contaminated diets may have been far more widespread than appreciated and mandates continued surveillance of primates in European zoos and breeding facilities.


            The 82 zoo animals with BSE:

            Id TSE Genus Species Subsp Birth Origin Death Place of Death
            654 x Microcebus murinus – 1997 U.Montpellier 1998 U.Montpellier
            656 x Microcebus murinus – 1997 U.Montpellier 1998 U.Montpellier
            481 + Eulemur fulvus mayottensis 1974 Madagascar 1992 Montpellier zoo
            474 + Eulemur fulvus mayottensis 1974 Madagascar 1990 Montpellier zoo
            584 – Eulemur fulvus mayottensis 1984 Montpellier 1991 Montpellier zoo
            455 + Eulemur fulvus mayottensis 1983 Montpellier 1989 Montpellier zoo
            – + Eulemur fulvus mayottensis 1988 Montpellier 1992 Montpellier zoo
            – + Eulemur fulvus mayottensis 1995 Montpellier 1996 Montpellier zoo
            – + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
            – + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
            – + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
            456 + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
            586 + Eulemur mongoz – 1979 Madagascar 1998 Montpellier zoo
            – p Eulemur mongoz – 1989 Mulhouse 1991 Montpellier zoo
            – p Eulemur mongoz – 1989 Mulhouse 1990 Montpellier zoo
            – p Eulemur macaco – 1986 Montpellier 1996 Montpellier zoo
            – p Lemur catta – 1976 Montpellier 1994 Montpellier zoo
            – p Varecia variegata variegata 1985 Mulhouse 1990 Montpellier zoo
            – p Varecia variegata variegata 1993 xxx 1994 Montpellier zoo
            455 + Macaca mulatta – 1986 Ravensden UK 1992 Montpellier zoo
            – p Macaca mulatta – 1986 Ravensden UK 1993 Montpellier zoo
            – p Macaca mulatta – 1988 Ravensden UK 1991 Montpellier zoo
            – p Saimiri sciureus – 1987 Frejus France 1990 Frejus zoo
            700 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            701 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            702 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            703 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            704 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            705 pc eulemur hybrid – – Besancon zoo 1998 Besancon zoo
            706 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            707 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            708 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            709 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            710 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            711 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            712 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            713 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            714 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            715 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            716 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            717 pc eulemur hybrid – – Strasbourg zoo 1998 Strasbourg zoo
            x p genus species – – Lille zoo 1996 Lille zoo
            y p genus species – – Lille zoo 1996 Lille zoo
            z p genus species – – Lille zoo 1996 Lille zoo

            1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU
            Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK
            Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK
            Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK
            Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR
            Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr
            xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR
            yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK
            zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK

            aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK
            yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK
            zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK

            xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK
            zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK

            85 + Felis catus cat 1990+ various 1999+ various UK LI NO
            19 + Canis familia. dog 1992+ various 1999+ various UK

            Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK
            yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK

            Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]

            1 + Taurotragus oryx eland 1987 Port Lympne 1989 Port Lympne zoo UK
            Moll + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
            Nedd + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
            Elec + Taurotragus oryx eland 1990 xx UK 1992 not Port Lympne Uk
            Daph p Taurotragus oryx eland 1988 xx UK 1990 not Port Lympne UK
            zzz + Taurotragus oryx eland 1991 zz UK 1994 zzz UK
            yyy + Taurotragus oryx eland 1993 yy UK 1995 yyy UK

            Fran p Tragelaphus strepsi. kudu 1985 London zoo 1987 London zoo UK
            Lind + Tragelaphus strepsi. kudu 1987 London zoo 1989 London zoo UK
            Karl + Tragelaphus strepsi. kudu 1988 London zoo 1990 London zoo UK
            Kaz + Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
            Bamb pc Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
            Step – Tragelaphus strepsi. kudu 1984 London zoo 1991 London zoo UK
            346 pc Tragelaphus strepsi. kudu 1990 London zoo 1992 London zoo UK
            324 + Tragelaphus strepsi. kudu 1989 Marwell zoo 1992 London zoo UK

            xxx + Tragelaphus angasi nyala 1983 Marwell zoo 1986 Marwell zoo UK

            yy + Oryx gazella gemsbok 1983 Marwell zoo 1986 Marwell zoo UK
            zz + Oryx gazella gemsbok 1994+ zzz zoo 1996+ zzzz zoo UK

            xx + Oryx dammah scim oryx 1990 xxxx zoo 1993 Chester zoo UK

            yy + Oryx leucoryx arab oryx 1986 Zurich zoo 1991 London zoo UK

            yy + Bos taurus ankole cow 1987 yyy zoo 1995 yyyy zoo UK
            zz + Bos taurus ankole cow 1986 zzz zoo 1991 zzzz zoo UK

            xx + Bison bison Eu bison 1989 xxx zoo 1996 xxxx zoo UK


            Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588

            Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320

            Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

            Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

            Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

            Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

            Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.

            Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444

            Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271

            Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.

            Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441

            Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.

            TSEs in Exotic Ruminants

            TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.


            Jeffrey, M. and Wells, G.A.H, (1988) Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet.Path. 25. 398-399

            Kirkwood, J.K. et al (1990) Spongiform encephalopathy in an Arabian oryx (Oryx leucoryx) and a Greater kudu (Tragelaphus strepsiceros) Veterinary Record 127. 418-429.

            Kirkwood, J.K. (1993) Spongiform encephalopathy in a herd of Greater kudu (Tragelaphus strepsiceros): epidemiological observations. Veterinary Record 133. 360-364

            Kirkwood, J. K. and Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.

            Food and Agriculture Organisation (1998) Manual on Bovine Spongiform Encephalopathy.

            so, i suppose we can agree, to disagree…

            kind regards,

  13. Virulence 4:4, 1–2; May 15, 2013; © 2013 Landes Bioscience


    Prion-resistant or prion-susceptible species, this is the question

    Comment on: Chianini F, et al. Proc Natl Acad Sci U S A 2012; 109:5080-5; PMID:22416127;


    Francesca Chianini,1 Natalia Fernández-Borges,2 Hasier Eraña,2 Yvonne Pang,2 Enric Vidal,3 Samantha L. Eaton,1 Jeanie Finlayson,1 Mark P. Dagleish1 and Joaquín Castilla2,4,*; 1Moredun Research Institute; Pentlands Science Park; Penicuik, Scotland UK; 2CIC bioGUNE; Parque tecnológico de Bizkaia; Bizkaia, Spain; 3Centre de Recerca en Sanitat Animal (CReSA); UAB-IRTA; Campus de la Universitat Autònoma de Barcelona; Barcelona, Spain; 4IKERBASQUE; Basque Foundation for Science; Bizkaia, Spain; *Email: castilla@joaquincastilla.com; http://dx.doi.org/10.4161/viru.24456

    Previous in vivo studies left the scientific community with the assumption that rabbits were resistant to prion diseases. However, our recent findings proved they are susceptible. The in vitro results were essential to demonstrate that prion protein (PrP) from every species has the potential to become not only misfolded to a disease associated form, but also capable of being virulent and causing clinical disease. Even though transmissible spongiform encephalopathies have only been described in mammals to date, it would not be too surprising if prion diseases could eventually be found in any class of animal that has PrP such as birds, reptiles or fish.

    The first reported observations of a transmissible spongiform encephalopathy (TSE) in Europe were in the first half of the 18th century when Thomas Comber described a disease of sheep, originally called rickets, which we know today as scrapie. However, the ability of TSEs to transmit to other species was unknown until 1960–1970 when the first experimental infections were performed in mice and other laboratory animals.

    The differences between TSEs and other contagious diseases were evident early on, starting with the unusual characteristics of their pathogenesis, their unknown origin and especially their ability to be transmitted experimentally to a large number of species, even though different species are not equally susceptible (Barlow et al., Res Vet Sci 1976).

    In the 1990s and early 21st century the main aim of TSE research was to establish the etiological agent, and although accomplishing this objective was of fundamental importance, it required most of the available funding resources and thereby prevented investigations of other aspects of these diseases.

    Whereas confirmation of the “protein only hypothesis” represented a significant step forward for TSE science, it made the strain phenomenon and transmissibility between species more difficult to explain. Undoubtedly, it would have been easier to explain TSEs if the etiological agent was a virus or a bacterium, instead of one whose principal or only component is a protein.

    In the past, many experimental infections were performed using different sources of TSEs, both within and between species, in an attempt to understand their pathogeneses and transmissibilities. However, in many occasions the existence of different strains was ignored.

    The appearance of bovine spongiform encephalopathy (BSE) advanced knowledge in this area as a large number of animals were accidentally exposed to a novel TSE agent (Bons et al., Proc Natl Acad Sci U S A 1999). This “unplanned experiment” also showed that not every species was equally susceptible. For example, BSE was found in the goat population in the UK and France, but no cases were reported in pigs, despite proven experimental susceptibility, and having been naturally exposed to the agent during the BSE outbreak. However, we should not generalize with respect to susceptibility to prion diseases as their behaviors, and possibly even their mechanisms, can be as numerous as the number of identified strains. Without knowledge of the intrinsic characteristic of strains, the observation of natural and experimental infections may lead us to think that every strain is a unique and independent agent. This is because, despite having several similar characteristics, sometimes the different TSE strains behave as differently as the influenza virus does from the hepatitis C viruses. For example, different TSE strains target different species and tissues, with different incubation times and result in different clinical manifestations. Due to these innate differences, predicting if a strain will transmit to another species is very difficult and suggesting that a disease associated prion protein generated in cows either can or cannot transmit to humans is also dangerous. At best, we can try estimating the zoonotic potential of animal prions with ad hoc models such as primates or human PrP transgenic mice. Furthermore, it is currently impossible to establish if and how these unconventional agents will adapt and mutate when they infect new species. For all these reasons it is ill-advised to define a species as resistant to prion diseases on the basis of absence of natural cases or experiments where one can only use a limited number of strains.

    The degree of pathogenicity of different disease associated prions, or virulence, is determined by the incidence of infection and the length of time between exposure and development of clinical signs. These data allow the classification of prion diseases from low to high virulence, but only if related to a specific species. This is because a TSE which is highly virulent in one species can be of low virulence or even avirulent in another. This paradigm of transmission is influenced by both the TSE strain and the species it is infecting, therefore, it is possible that every species has a specific strain that, once adapted, would represent the most virulent disease associated prion in that species.

    The route of infection in TSEs plays a critical role in transmissibility and also the capacity of prions to replicate extraneurally is strainspecific (Beringue et al., Science 2012). This is often also responsible for the virulence of a strain in the same species. An exceptional example of transmissibility is scrapie, which, despite having been recognized for centuries as being highly virulent in sheep and goats, has never been reported as a natural infection in any other species and is therefore considered avirulent in humans. However, no one can be totally sure about its ability to adapt to other species. With respect to this it is important to mention that when BSE has been transmitted to sheep it becomes more virulent on re-passage as denoted by shorter incubation times in cattle and by an increase in the number of species it is capable of infecting (Padilla et al., PLoS Pathog 2011). These changes could happen with other TSE strains.

    It is interesting to consider the potential virulence in common domestic species in which spontaneous prion diseases have never been reported. We should be very cautious in predicting the behavior of TSEs in these animals as transmissibility will depend on the combination of strain and challenged species. Nevertheless one should not consider this area of research an unanswerable enigma unless all strains are tested in every species, as this is unrealistic. To resolve this situation and start addressing some of these questions we have used our expertise in the in vitro replication of prions (Castilla et al., Cell 2005). We have examined a large number of TSE strains/ challenge species transmission combinations and performed a two passage study on the susceptibility of rabbits to in vitro generated homologous species disease associated prion infection (Chianini et al., Proc Natl Acad Sci U S A 2012). Prior to this study there were many uncertainties with respect to the susceptibility of rabbits to TSEs; previous in vivo studies had failed to transmit the disease yet the success of our in vitro studies proved that rabbit PrP could be efficiently misfolded after being seeded with different prion strains from different species and even formed an infectious de novo strain from unseeded brain.

    The results of the in vivo studies left the scientific community with the assumption that rabbits were resistant to prion diseases. However, our recent findings proved they are susceptible. The in vitro results were essential to demonstrate that PrP from every species has the potential to become not only misfolded to a disease associated form, but also capable of being virulent and causing clinical disease. In our case rabbit PrP misfolded in vitro and produced a de novo proteaseresistant PrP from a healthy rabbit brain. This de novo PrP was capable of infecting a small percentage of rabbits on primary passage but a very high percentage succumbed to clinical disease upon second passage. Although with respect to our definition of virulence we could not consider our strain to be highly virulent; the mean for the incubation time was around 550 d post infection, we should not forget that several factors can influence the incubation time without altering the virulence. A clear example of this would be the long incubation times associated with human TSE strains in human infections, which are highly virulent.

    From the production of the de novo TSE strain derived from the brain of a healthy rabbit it is tempting to speculate that its formation may be comparable to the spontaneous forms of prion disease, called atypical, and reported in humans and ruminants. These forms of prion diseases have always proven to be efficiently transmitted to the homologous species.

    Even though we demonstrated that rabbits are not resistant to prion diseases, the studies performed in vivo previously and then confirmed with our study, showed that this species is not susceptible to TSE strains commonly virulent in other species such as ME7 in mice. These findings highlight the importance of the compatibility between the infectious PrP and the native PrP of the challenged species. This compatibility is dependent upon the amino acid sequence of the PrP and differences between the two proteins can determine the success or not of replication of the disease associated form.

    Unfortunately, a simple comparison of PrP amino acid sequences between the species where strains have originated and the ones which are to be investigated cannot determine which PrP amino acids are responsible for successful disease transmission. This is not surprising since different strains with a different clinical course can be raised from the same species which has the same PrP amino acid sequence. To make things more complex, intermediate hosts can change the ability of certain prion diseases to become infectious in a species that otherwise appears not to be susceptible. The mechanism of how this happens is unclear, but the intermediate host may induce a conformational change or a mutation in the disease associated PrP strain or just aid the infectious ability of this strain in a different PrP environment. Therefore, thanks to intermediate hosts, certain TSE strains can increase their virulence and spread to other species as happened for BSE transmitted to sheep as previously explained.

    In conclusion, even though TSEs have only been described in mammals to date, it would not be too surprising if, given the chance to evolve through intermediate hosts, prion diseases could eventually be found in any class of animal that has PrP such as birds, reptiles or fish.


    News & Views

    Prion-resistant or prion-susceptible species, this is the question

    Comment on: Chianini F, et al. Proc Natl Acad Sci U S A 2012; 109:5080-5; PMID:22416127; http://dx.doi.org/10.1073/pnas.1120076109 Francesca Chianini,1 Natalia Fernández-Borges,2 Hasier Eraña,2 Yvonne Pang,2 Enric Vidal,3 Samantha L. Eaton,1 Jeanie Finlayson,1 Mark P. Dagleish1 and Joaquín Castilla2,4,*; 1Moredun Research Institute; Pentlands Science Park; Penicuik, Scotland UK; 2CIC bioGUNE; Parque tecnológico de Bizkaia; Bizkaia, Spain; 3Centre de Recerca en Sanitat Animal (CReSA); UAB-IRTA; Campus de la Universitat Autònoma de Barcelona; Barcelona, Spain; 4IKERBASQUE; Basque Foundation for Science; Bizkaia, Spain; *Email: castilla@joaquincastilla.com; http://dx.doi.org/10.4161/viru.24456


  14. Saturday, May 25, 2013

    Wyoming Game and Fish Commission Alkali Creek Feedground #39126 Singeltary comment submission


    kind regards,

    • Ron says:

      Terry, How do we know that CWD is always a fatal disease if we do not have a live animal test ??? Could there be such a thing as a CWD carrier deer or elk that never dies from CWD ???

      • Ron says:

        May 26, 2013 at 6:52 am

        Terry, How do we know that CWD is always a fatal disease if we do not have a live animal test ???

        reminds me of, if a bear zhits in the woods, or if a tree falls in the forest 😉 just kidding, good question…TSS

        Prion diseases are usually rapidly progressive and always fatal.




        Could there be such a thing as a CWD carrier deer or elk that never dies from CWD ???

        yes. …TSS

        Hi Ron,

        to date, all TSE prion disease are 100% fatal, once clinical. on the other hand, one can be subclinical, and die from another disease or another reason. CWD TSE prion disease are a long term, long incubating disease.

        however, if you live long enough, the TSE prion disease will eventually terminate you. there has been many studies to confirm this in animals, and a few in humans, that were hooked up to machines, but in the end, the TSE prion disease terminated them all, that have been clinical. you can be sub-clinical, and not knowing, pass it forward, to expose and infect others, but yet in some instances, die from something else, yet you may have exposed countless others.

        different species, different genetic make up, different routes, different sources, different titre of infectivity and the load there from, amplification, accumulation, then we now have to add into the formula, the atypicals, the different strains there from, it really gets interesting.

        we now have the prionopathies, the tauopathies, the proteinopathies, oh my, when in the end, in my opinion, they might very well be a TSE, a Transmissible Spongiform Encephalopathy, except when all the above factors are added up, for each one, they just add someone’s name to it, or another CJD, xxxopathy, Alzheimers, ALS, Parkinsons, Picks, and countless others, if they become transmissible, Houston, then we have a serious problem. they can’t continue to have their cake, and eat it too.

        something is to explain all these diseases, or this one disease.

        what is Alzheimer’s for instance?

        where did it come from, and when?

        about the same time as Creutzfeldt Jakob Disease or Jakob Creutzfeldt Disease, depending on who you think discovered it first, Mr. Jakob or Mr. Creuztfeldt or Mr. Heidenhain ? or others ? simply names, for the same disease, TSE prion disease. how many more ?

        just my opinion… please see ;


        Recently, PrPTSE and its proteinaceous seeding activity could be directly demonstrated, for the first time, in skeletal muscles of CWD-infected cervids.10 The animals examined in this study were farmed and free-ranging WTD for which no clinical signs of CWD had been recognized. However, they had been officially confirmed positive for CWD based on the detection of PrPTSE in brain tissue or lymph nodes and were thus apparently in a state of pre or subclinical infection. Muscles from such clinically inconspicuous carrier animals appear more likely to enter the human food chain than meat from cervids that show symptoms of CWD. Whether this may provide a relevant mode for the inadvertent foodborne transmission of CWD prions is still unclear. Yet, the presence and seeding activity of PrPTSE in skeletal muscles of pre- or subclinically infected WTD reinforced the need to comprehensively assess whether humans are susceptible to zoonotic CWD infections.


        Transmissibility to humans

        The current state of epidemiological research suggests a rather robust barrier for the transmission of CWD to humans. Particularly, the surveillance of human prion diseases in areas with a long history of endemic CWD such as Colorado and Wyoming did not reveal evidence for zoonotic transmissions of the disease to cervid hunters or consumers of meat from elk and deer.6,11 However, as discussed by Belay et al.,6 the intensity of human exposure to CWD prions may increase due to a further spread and rising prevalence of the disease in cervids. Therefore, and with the generally long latency periods of human prion diseases in mind, previous epidemiological findings cannot be readily extrapolated. Until recently, experimental studies that pursued biochemical approaches or used transgenic mice to ascertain the susceptibility of humans to CWD infections consistently seemed to corroborate current epidemiological findings: CWD-infected cervid brain tissue did not seed the conversion of PrPC 133 into PrPres in PMCA assays using brain homogenate from macaques or transgenic mice expressing human PrPC as test substrate12 , and transgenic mice overexpressing human PrPC were resistant to infection after intracerebral challenge with CWD prions from mule deer.13 However, a study published by Barria et al.14 in March 2011 found that cervid PrPTSE can seed the conversion of human PrPC into PrPres by PMCA when the CWD agent has been previously passaged in vitro or in vivo. Specifically, this was demonstrated for CWD prions from naturally affected mule deer either passaged by serial PMCA using deer PrPC as conversion substrate or in transgenic mice expressing cervid PrPC. The authors of this study pointed out that CWD prions may undergo a gradual process of change and adaptation via successive passages in the cervid population. They concluded that the reported findings, if corroborated by infectivity assays, may imply “that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading”.



        Saturday, May 25, 2013

        Brain homogenates from human tauopathies induce tau inclusions in mouse brain


        Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.





        Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

        The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.



        Prion Transmission from Cervids to Humans is Strain-dependent

        Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

        Key words: CWD, strain, human transmission

        Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

        Acknowledgement Supported by NINDS NS052319 and NIA AG14359.


        Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

        Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer’s disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

        Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.


        Biochemical and Biophysical Characterization of Different CWD Isolates

        Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany

        Key words: CWD, strains, FT-IR, AFM

        Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.



        Wednesday, September 08, 2010



        Saturday, March 09, 2013

        Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases


        Overview of Prion Diseases Transmissible spongiform encephalopathies (TSEs) are a group of related diseases including Creutzfeldt-Jacob disease (CJD) and its new variant (vCJD), kuru (all three affect humans), scrapie in sheep and goats, bovine spongiform encephalopathy (BSE; “mad cow disease”), and chronic wasting disease (CWD) in deer and elk. These diseases have long incubation periods of years or decades, cause progressive neurological degeneration, evoke no obvious inflammation or immune response, and are invariably fatal.


        Prion disease in sheep, known as scrapie, has been recognized for centuries and controlled by removing infected animals from herds (culling). When BSE was identified in cattle in the 1980s, it was also controlled by culling infected animals. Prion diseases in humans are relatively rare. The incidence of CJD in humans is about 1 in 1 million; about 10% of such cases are inherited. However, the potential impact of prion diseases on human health was greatly magnified by the recognition that the transfer of BSE in cows to humans by beef ingestion resulted in vCJD. Changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, but there is concern that CWD of free-ranging deer in the United States might be transferred from deer to humans through venison consumption. Whether BSE and CWD represent a transfer of scrapie in sheep to cows and deer or are newly arisen prion diseases is unknown. The possible transmission of prion disease through other food animals also cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. It is possible that an unknown number of asymptomatic individuals are infected with vCJD from BSE, CWD, or scrapie. This potential threat to blood and plasma supplies is of great concern to both civilian and military health professionals.


        kind regards,

        • WM says:

          Terry’s extensive bibliography and quotes from various (sometimes conflicting)studies is enlightening.

          Will CWD ever jump a species to infect humans?

          I am not, nor ever have been, a fan of former Secretary of Defense Rumsfeld. However, he made a speech about “unknown unknowns,” that is food for thought.

          A Psychology Today author took the concept one step further (and if you read the article you may recall the cartoon character, Mr. Magoo, from the 1970’s:


          Are we really smart enough to know weighing the risks of CWD and the consequences?

    • Ralph Maughan says:


      Thanks for letting us know about the feedground renewals. We have fought them before, but it is very hard to get the ear of the officials. I believe that this is because Wyoming sort of has an elk feeding industry. That industry seems as resistant to inactivation as do prions on the soil.

      One of the reasons Wyoming Game and Fish hated the wolves so early was that they hung near the feedlots in the winter. Yes, they ate all the elk they wanted, but more irritating to Wyoming was that they disturbed their alfalfa distribution program by moving the elk up or down the Gros Ventre River drainage.


May 2013


‎"At some point we must draw a line across the ground of our home and our being, drive a spear into the land and say to the bulldozers, earthmovers, government and corporations, “thus far and no further.” If we do not, we shall later feel, instead of pride, the regret of Thoreau, that good but overly-bookish man, who wrote, near the end of his life, “If I repent of anything it is likely to be my good behaviour."

~ Edward Abbey